Inbred strains of mice are generally unable to make an antibody response to the synthetic copolymer (glu[unreadable]50[unreadable]tyr[unreadable]50[unreadable]) (GT). We have previously shown that this unresponsiveness is not due to a B-cell defect. Some strains of mice develop GT-specific suppressor cells (Ts) and specific suppressor factors (TsF) in response to GT challenge. This phenomenon is controlled by genes located in the major histocompatibility complex (H-2). Cyclophosphamide treatment of "GT-suppressor" strains of mice will allow them to respond to subsequent GT challenge by the production of GT-specific, plaque-forming cells (PFC). Moreover, cyclophosphamide treatment of suppressor strain mice (H-2[unreadable]k,d[unreadable]) allows these strains to make GT-specific helper cells and helper factors. We are characterizing the nature of these GT-specific helper cells (possibly Th) and their helper factors (which we are provisionally terming ThF). Currently these cells are being maintained in tissue culture as continuous T-cell lines. The cells appear to bear Thy-1 markers and, thus, would appear to be T cells. These T-cell lines, when transferred to Mishell-Dutton-type cultures, appear to help naive spleen cells (syngeneic) make a GT-specific PFC response. Moreover, soluble products of these T-cell lines appear to have helper activity. The helper material (ThF) binds to GAT-\or GT-Sepharose immunoadsorbent columns and does not bind to columns of irrelevant antigens. The eluates from these columns (i.e., those which are specifically bound by the column, then eluted with an acid buffer) help GT but not anti-SRBC, PFC responses. We plan to further characterize the cellular origin of the ThF and characterize its antigenic markers (idiotype, I-A, etc.) and the cellular target for the ThF in the coming grant year. Our experiments will be performed initially in vitro and will then be confirmed in in vivo models. (LB)